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Ultrasonography for diagnosis of obstructing ureteral calculus.

The reliability of ultrasonography in diagnosing ureteral obstruction caused by calculus was prospectively investigated. In 60 consecutive cases sonograms were compared with excretory urograms. The sonographic diagnosis was correct in 27 (79%) of the 34 cases shown by urography to have ureteral obstruction, and the sonograms showed the causal calculus in 17. The rate of false negative sonographic diagnosis was thus 21%. In two patients with no urographic abnormality, the sonograms indicated ureteral calculus without signs of obstruction. Ultrasonography may be used as an alternative to emergency urography for initial imaging in cases of suspected ureteral obstruction, but urography remains the standard method for evaluating the obstructed urinary tract, due to its greater accuracy and ability to assess renal function.

Adolescent↗

The management of malignant ureteral obstruction treated with ureteral stents.

PURPOSE: We developed an algorithm for the management of ureteral obstruction due to malignant extrinsic compression. MATERIALS AND METHODS: We retrospectively reviewed all ureteral stents placed for noncalculous reasons at our institution from January 1, 1990 to January 1, 2004. Further clinical information was gathered from 157 patients with malignant extrinsic ureteral compression. Failure was defined as recurrent ureteral obstruction or an inability to place stents cystoscopically. RESULTS: A total of 157 patients underwent retrograde ureteral stent attempt for malignant extrinsic ureteral obstruction. Mean patient age was 54.7 years (range 23 to 83) and average followup was 13.6 months. Of our patients 61% were women, and the most common cancer diagnoses were ovarian cancer (in 26), lymphoma (17) and cervical cancer (16). A total of 24 patients required immediate percutaneous nephrostomy (PCN) referral. There were 32 patients who experienced a late failure and required PCN (average 180 days after initial stent), and 83 patients in our series (52.9%) who experienced 110 major complications. Type of cancer did not predict need for PCN. However, when invasion into the bladder was noted on cystoscopy, 55.9% (19 of 34, p = 0.008) progressed to PCN referral. A total of 77 patients underwent stent replacement on average 2.8 times and with an interval of 95 days. CONCLUSIONS: In our series patients with malignant extrinsic ureteral compression presenting for ureteral stent(s) experienced a failure rate of 35.7% (56 of 157). Invasion at cystoscopy had a significant predictive value for progression to PCN. We present an algorithm on the management of extrinsic malignant ureteral obstruction.

Adult↗

Renal tubular apoptosis after partial ureteral obstruction.

Partial ureteral obstruction in the weanling rat leads to hydronephrosis of the ipsilateral kidney and renal cell deletion through the process of programmed cell death known as apoptosis. The apoptotic response following partial ureteral obstruction in weanling Sprague-Dawley rats was studied using the traditional markers of apoptosis, including deoxyribonucleic acid (DNA) laddering pattern on agarose gel electrophoresis, in situ gap labeling of fragmented DNA for quantitative apoptotic body determination, polyadenylated messenger ribonucleic acid (mRNA) expression of sulfated glycoprotein-2, and polyadenylated mRNA expression of epidermal growth factor and transforming growth factor-beta. Partial ureteral obstruction resulted in a progressive increase in the intensity of DNA fragmentation associated with apoptosis during the initial 3 weeks. Quantitative apoptotic body counting revealed a 3-fold increase by week 3 of partial obstruction. This increase represented a level of apoptosis, which is 65% of that observed in complete ureteral obstruction. By week 2 of partial obstruction there was a 13-fold increase in the expression of sulfated glycoprotein-2 mRNA, as well as changes in the growth factor environment characterized by a decline in the constitutive expression of epidermal growth factor mRNA and an increase in the expression of transforming growth factor-beta mRNA. These altered levels represent changes in expression comparable to those observed during the apoptotic response following complete ureteral obstruction, although the time course is delayed by 2 to 3 weeks.

Animals↗

15-year experience with the management of extrinsic ureteral obstruction with indwelling ureteral stents.

PURPOSE: We assessed the success of retrograde placement of indwelling ureteral stents in the management of ureteral obstruction due to extrinsic compression. MATERIALS AND METHODS: Between July 1987 and December 2002 adequate followup was available for 101 patients who underwent primary retrograde ureteral stenting for extrinsic ureteral obstruction. Mean age at presentation was 61.4 years (range 33 to 90). Chart review was performed on all patients for primary diagnosis, symptomatology, degree of hydronephrosis, creatinine levels (baseline, treatment and posttreatment), location of compression, size and number of stents used, progression to percutaneous nephrostomy tube (PNT), stent failure, days to stent failure, post-stent therapy and status at last followup. RESULTS: Mean length of followup was 11 months (range 1 to 127). In 101 patients 138 ureteral units (UU) were stented. Total stent failure occurred in 41 (40.6%) patients and 58 (42.0%) UU. A total of 40 (29.0%) UU required PNTs at a mean of 40.3 days (range 0 to 330) with 18 PNTs placed in less than 1 week. Cases of stent failure that did not undergo PNT placement included 18 (13.0%) UU at a mean of 52.4 days (range 3 to 128). A total of 90 (89.1%) patients had metastatic cancer at stenting with 32.2% dead at 5.8 months (range 1 to 32). Univariate and multivariate analyses identified cancer diagnosis, baseline creatinine greater than 1.3 mg/dl and post-stent systemic treatment as predictors of stent failure. Proximal location of compression and treatment creatinine greater than 3.11 mg/dl were marginal predictors of failure on univariate analysis, while proximal location of obstruction was also marginally significant on multivariate analysis. No predictors were identified for early stent failure (less than 1 week). CONCLUSIONS: At almost 1 year followup stent failure due to extrinsic compression occurred in nearly half of treated patients. Analysis of data revealed a diagnosis of cancer, baseline mild renal insufficiency and metastatic disease requiring chemotherapy or radiation as predictors of stent failure. Managing extrinsic compression by retrograde stenting continues to be a practical but guarded decision and should be tailored to each patient.

Adult↗

Electrical properties of the rabbit cortical collecting duct from obstructed kidneys after unilateral ureteral obstruction. Effects of renal decapsulation.

Ureteral obstruction causes impaired salt wastage and K+ secretion in the distal nephron segments, including the cortical collecting duct (CCD). Recently, we demonstrated that conductances of Na+ and K+ in the apical membrane, as well as the electrogenic Na(+)-K+ pump activity and the relative K+ conductance in the basolateral membrane of the collecting duct cell, were inhibited in the obstructed kidney after unilateral ureteral obstruction (UUO). To examine whether the increased intrarenal pressure might be causally related to these abnormalities in the CCD, the effects of unilateral renal decapsulation, a maneuver that partially blocks the increase in renal pressure, were evaluated with microelectrode techniques in isolated CCDs from UUO and sham-operated (control) rabbits 24 h after operation. Renal decapsulation had no effects on barrier voltages and conductances in the CCD from control animals. The lumen-negative transepithelial (VT) and basolateral membrane (VB) voltages as well as the transepithelial (GT) and the apical membrane (GA) conductances were decreased in the CCD from UUO animals compared with control animals. Pretreatment of renal decapsulation partially corrected the decreases in VT, VB, GT, and GA seen in the CCD from UUO animals. The changes in apical membrane voltage and GT upon addition of luminal amiloride and Ba2+, and the changes in VB upon addition of bath ouabain, were also decreased in the CCD from UUO animals compared with control animals. Pretreatment of renal decapsulation also partially corrected the above abnormalities seen in UUO animals, whereas it had no effect in control animals. The transference numbers for Cl- (tCl) and K+ (tK) in the basolateral membrane were, respectively, increased and decreased in the CCD from UUO animals compared with control animals. Pretreatment of renal decapsulation also partially corrected the changes in tCl and tK seen in UUO animals, whereas it had no effect in control animals. We conclude that, in UUO animals, renal decapsulation partially corrects the inhibition of apical Na+ and K+ conductances as well as basolateral Na(+)-K+ pump activity and relative K+ conductance seen after UUO, whereas in control animals it has no effect. The increased renal pressure may partly contribute to the defects in Na+ and K+ transport in the CCD from obstructed kidneys. Renal decapsulation has protective effects on impaired Na+ and K+ transports in the CCD after ureteral obstruction.

Animals↗

Modulation of apoptotic and inflammatory genes by bioflavonoids and angiotensin II inhibition in ureteral obstruction.

OBJECTIVES: Ureteral obstruction results in an injury response that can progress to irreversible renal fibrosis and tubular atrophy by apoptosis. The molecular events leading to apoptosis from obstruction are not well understood. We investigated the effect of bioflavonoids and angiotensin II inhibition on apoptotic and inflammatory gene expression in a model of unilateral ureteral obstruction (UUO). METHODS: Complete UUO was produced in rats by ureteral ligation. The rats were treated with dimethyl sulfoxide (control), enalapril, losartan, curcumin, or quercetin. The animals were killed on day 7 and both obstructed and contralateral unobstructed kidneys were harvested. Expression of the inflammatory chemokine monocyte chemotactic protein-1, apoptosis effector genes Fas and Fas ligand, and oxidative stress gene HO-1 was evaluated by reverse transcriptase-polymerase chain reaction. RESULTS: Ureteral obstruction was associated with a 6.3-fold increase in monocyte chemotactic protein-1 expression compared with sham-operated rats (P = 0.01). Monocyte chemotactic protein-1 expression was severely attenuated in all other treatment groups (P <0.05). Similarly, Fas and Fas ligand expression were increased in control UUO kidneys compared with sham-operated ones (P <0.05). Fas gene expression was significantly inhibited by quercetin but not enalapril, losartan, or curcumin compared with the control. The induction of Fas ligand was attenuated in all treatment groups (P <0.05). HO-1 was expressed at low levels in both unobstructed and obstructed kidneys. Treatment with curcumin increased HO-1 expression fourfold (P <0.05). CONCLUSIONS: The expression of apoptotic and chemokine genes is significantly upregulated in UUO. Bioflavonoids and angiotensin inhibitors are able to attenuate the expression of these genes and thus may be beneficial in renal protection.

Angiotensin II↗

Postoperative ureteral obstruction after confirmed ureteral patency: a case report.

Ureteral injury after pelvic floor surgery and anti-incontinence surgery is a well-known risk. It is common practice to evaluate ureteral patency immediately after surgery prior to leaving the operating theater to assure that the ureters are open and functional. In this report we discuss the case of a patient who was admitted 9 days after surgery with acute onset of ureteral obstruction after having patent ureters documented at the time of surgery. A literature search failed to show any documented cases.

Diagnosis, Differential↗

[Percutaneous endourologic treatment of obstructive ureteral lithiasis in renal transplant].

Donor graft lithiasis is a unusual complication of renal transplantation, however, it is associated to a high morbidity. This pathology is due to several causes such us: metabolic factors, infectious disease, drugs, foreign bodies or transferred in the donor graft. The objective of the treatment is to remove the lithiasis without damaging the renal unit. We report the successful percutaneous anterograde treatment of an ureteral obstructive hard calculi, in renal allograft.

Humans↗

Reimplantation of the ureter in prostatic carcinoma associated with bilateral ureteric obstruction.

Bilateral ureteric obstruction from prostatic carcinoma is not uncommon. A number of techniques for urinary diversion have been used in selected patients when uraemia develops. Reimplantation of the ureter(s) as an alternative to urinary diversion has been carried out in 21 patients over a 7-year period. In 6 of these patients bilateral reimplantation was done. In another 6 patients reimplantation of the ureter was not possible and cutaneous ureterostomy was carried out. The overall survival time was 10.6 months. In 13 patients living more than 6 months post-operatively, survival time was 1.8 years. Most patients had severe uraemia and advanced (clinical stage III or IV) prostatic carcinoma. The immediate management of these patients is outlined and the importance should be considered is stress. It is concluded that, whenever possible, ureteric reimplantation should be considered for relieving ureteric obstruction in patients selected for active treatment.

Aged↗

Expression of LFA-1 (CD11a/CD18) and ICAM-1 (CD54) in an animal model of renal interstitial fibrosis induced by unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) has been used as an experimental model to induce tubulointerstitial damage and interstitial fibrosis. UUO is characterized by cellular proliferation, accumulation of inflammatory cells, and subsequent replacement of renal parenchyma by fibrous tissue. The influx of inflammatory cells into the renal interstitium is mediated by adhesion molecules. In this study, the development of fibrosis in the UUO model of the rat was examined and its relation to the time course of LFA-1 and ICAM-1 expression was assessed by immunohistochemistry. An increase in interstitial connective tissue was detected on day 10 after UUO, with a maximum on day 35. After unilateral ureteral obstruction, LFA-1 was prominently expressed in interstitial infiltrates, and to a lesser degree in glomerular areas. An initial increase in LFA-1-positive cells was noted already on day 10, with a maximum on day 20 and a decline on day 25. During the time course of 35 days after UUO, we observed an increase in ICAM-1 expression in the vascular endothelium, in tubular epithelium and in interstitial areas. This study shows that LFA-1 expression and ICAM-1 expression are concordant and that this process is associated with increasing interstitial fibrosis. ICAM-1 interstitial tissue may facilitate the homing and persistence of an interstitial infiltrate by ICAM-1/LFA-1 interactions, thereby preceding the development of renal interstitial fibrosis.

Animals↗

Predicting the success of retrograde stenting for managing ureteral obstruction.

PURPOSE: Retrograde ureteral stenting is often considered the first line option for relieving ureteral obstruction when temporary drainage is indicated. Several retrospective studies have implied that in cases of extrinsic obstruction retrograde ureteral stenting may fail and, therefore, percutaneous nephrostomy drainage is required. We examined the efficacy of retrograde ureteral stenting for resolving ureteral obstruction and identified clinical and radiological parameters predicting failure. MATERIALS AND METHODS: Enrolled in our prospective study were 92 consecutive patients with ureteral obstruction, which was bilateral in 8. Retrograde ureteral stenting was attempted in all cases by the urologist on call. When stent insertion failed, drainage was achieved by percutaneous nephrostomy. Patients were followed at 3-week intervals for 3 months. Each followup visit included a medical interview, blood evaluation, urine culture and ultrasound. Stent malfunction was defined as continuous flank pain manifesting as recurrent episodes of acute renal colic, 1 or more episodes of pyelonephritis, persistent hydronephrosis or elevated creatinine. Preoperative data and outcomes were compared in cases of intrinsic and extrinsic obstruction. Univariate and multivariate analysis was done to identify predictors of the failure of ureteral stent insertion and long-term function. RESULTS: The etiology of obstruction was intrinsic in 61% of patients and extrinsic in 39%. Extrinsic obstruction, which was associated with a greater degree of hydronephrosis, was located more distal. Retrograde ureteral stenting was successful in 94% and 73% of patients with intrinsic and extrinsic obstruction, respectively. At the 3-month followup stent function was maintained in all patients with intrinsic obstruction but in only 56.4% with extrinsic obstruction. On multivariate logistic regression the type of obstruction, level of obstruction and degree of hydronephrosis were the only predictors of stent function at 3 months. Stent diameter and preoperative creatinine had no predictive value. CONCLUSIONS: Retrograde ureteral stenting is a good solution for most acutely obstructed ureters. In patients with extrinsic ureteral obstruction a more distal level of obstruction and higher degree of hydronephrosis are associated with a greater likelihood of stent failure. These patients may be better served by percutaneous drainage.

Adult↗

Angiotensin receptor blockade decreases fibrosis and fibroblast expression in a rat model of unilateral ureteral obstruction.

PURPOSE: Unilateral ureteral obstruction is characterized by histopathological changes including interstitial fibrosis, fibroblast specific protein expression, tubular atrophy and apoptosis, and macrophage infiltration. Angiotensin II has been implicated in some of these changes. We examined the effect of angiotensin blockade on markers of renal injury, including fibroblast specific protein expression, fibrosis, apoptosis and macrophage infiltration. We used losartan, an angiotensin II antagonist, in a unilateral ureteral obstruction model and studied animals 3 weeks after unilateral ureteral obstruction, a time at which renal damage is well established. MATERIALS AND METHODS: Rats underwent unilateral ureteral obstruction and were given either drinking water or losartan for 21 days. Kidneys were harvested and examined for fibrosis (trichrome and the Sircol assay for collagen), apoptosis (TUNEL), and fibroblast specific protein expression and macrophage infiltration (immunohistochemistry). RESULTS: Unilateral ureteral obstruction was found to induce fibrosis, apoptosis, fibroblast expression and macrophage in the obstructed kidney. Losartan significantly decreased apoptosis and macrophage infiltration in the obstructed kidney. It also decreased fibrosis, as measured by either trichrome staining assessed by a pathologist, the Sircol assay for collagen or fibroblast specific protein expression. However, approximately 50% of the changes were not affected by the current treatment, suggesting that other factors contribute to renal damage in unilateral ureteral obstruction. CONCLUSIONS: We observed the direct contribution of angiotensin II to both apoptotic and cellular transition processes (epithelial mesenchymal transition) and fibrosis in unilateral ureteral obstruction. Because these processes are active not only in unilateral ureteral obstruction, but also in other renal diseases, the value of angiotensin II blockade as an important part of the antifibrotic armamentarium has been confirmed.

Angiotensin II Type 1 Receptor Blockers↗

Paradoxical tubular obstruction after release of ureteral obstruction in rat kidney.

The healing process of hydronephrosis was studied using rat kidney. Following release of 2 weeks' unilateral hydronephrosis, renal papilla and cortex were examined by scanning electron microscopy. Shortly after the release of obstruction, massive loss of brush border and ballooning of epithelial cells were noted in proximal tubules. Distal tubules and collecting tubules also showed severe ballooning of epithelial cells. Actually most of them were completely or nearly obliterated in spite of the release of ureteral obstruction. Two weeks later, on the other hand, the many tubular components became patent with normal epithelial lining. Some of them, however, deteriorated further in spite of the release of obstruction. Thus there was a marked tubular heterogenicity in recovery. The sudden decrease of the pelvic pressure and chronic ischemic state during ureteral obstruction may cause the tubular changes which were observed in this study.

Animals↗

Renal injury and recovery in partial ureteric obstruction.

Partial ureteric obstruction was produced by insertion of an obstructing stent into the left ureter of 21 mongrel dogs and the duration of obstruction was varied as follows: Group A (n = 7) for 60 days; Group B (n = 7) for 28 days; Group C (n = 7) for 14 days. Intrapelvic pressure monitoring confirmed that obstruction had been produced by stent insertion and relieved by reimplantation of the left ureter following the designated obstruction period. The extent of recovery of renal function was assessed by creatinine clearance, with group C maintaining normal function, group B recovering 31% and group A recovering 8% of control function. Methyl-methacrylate extrusion casts of the renal microvasculature were made in group B and C kidneys and studied by scanning electron microscopy. During obstruction there was evidence of arteriolar constriction. These changes provide a morphological basis for the renal functional alterations and support the concept that post-obstructive renal failure is a vascular injury.

Animals↗

Renal cortical release of a specific macrophage chemoattractant in response to ureteral obstruction.

Acute ureteral obstruction results in a large influx of macrophages into the cortex and medulla of the obstructed kidney. We examined supernatants from short-term cultures of acutely obstructed and contralateral control renal cortices to determine whether differential production of a chemoattractant for macrophages could account for the cellular infiltrate observed in the obstructed kidney. Using a microchemotaxis assay, supernatants from obstructed renal cortex did demonstrate significantly more chemotactic activity for rat peritoneal macrophages than did supernatants from the contralateral kidneys. This activity showed a dose-response relationship with macrophage migration, peaked between 4 and 12 hours of obstruction, and declined with longer periods of obstruction. The activity was heat stable. It was retained by an octadecylsilane column, and eluted with methanol. Partitioning of the methanol fraction into aqueous and organic phases demonstrated significant activity in the organic phase. In summary, the acutely obstructed rat kidney releases a previously undescribed chemotactic factor that behaves as a lipid. This factor may account for the mononuclear cell infiltrate observed during obstruction.

Animals↗

[Pancreatitis: a little-known cause of ureteral obstruction].

Left ureteral stenosis induced by pancreatitis was observed in one case. Five similar cases have been reported in the literature. Ureteral obstructions may be found in two clinical contexts--patent pancreatitis or retroperitoneal fibrosis. The ureter may be simply compressed mechanically, or there may also be enzymatic or ischemic necrosis. The clinical approach should be directed towards treating primarily the pancreatitis and secondarily the urological pathology. As regards the urological treatment, ureterolysis or ilio-ureteroplasty are indicated in cases of organized irreversible ureteral stenosis.

Adult↗

Angiotensin II receptor antagonist ameliorates renal tubulointerstitial fibrosis caused by unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) results in tubulointerstitial fibrosis of the obstructed kidney (OBK). In this study we report that a specific angiotensin II (Ang II) receptor antagonists, SC-51316, ameliorates the expansion of the renal cortical interstitium in the OBK of the rat at five days of UUO. This is similar to the effect of an angiotensin converting enzyme (ACE) inhibitor, enalapril. SC-51316 (20 mg/liter in the drinking water) or enalapril (200 mg/liter in the drinking water) was administered beginning 24 hours before UUO and continued through five days after UUO. The relative volume of the tubulointerstitium (Vv) was measured by a point-counting method, and monocyte/macrophage infiltration, alpha smooth muscle actin (alpha SMA), proliferating cell nuclear antigen (PCNA), and collagen type IV (collagen IV) protein deposition were examined histologically using specific antibodies. We also examined the mRNA levels of transforming growth factor beta 1 (TGF-beta 1) and collagen IV by reverse transcription polymerase chain reaction. In untreated rats with UUO, Vv was remarkably expanded; collagen IV and alpha SMA protein deposition in the interstitium and PCNA labeling of nuclei were increased. These changes were significantly ameliorated by administration of an ACE inhibitor or an Ang II receptor antagonist. A monocyte/macrophage infiltration was evident in the OBK of untreated or Ang II receptor antagonist treated rats but was greatly reduced in the OBK of rats given enalapril. Increased expression of TGF-beta 1 mRNA and collagen IV mRNA was blunted (40 to 75%) by the administration of Ang II receptor antagonist or enalapril. The Ang II receptor antagonist or the ACE inhibitor did not affect the contralateral kidney of rats with UUO or the control kidney of normal rats. This study indicates that the renin-angiotensin system has a major role in the pathogenesis of the tubulointerstitial fibrosis of obstructive nephropathy. The tubulointerstitial fibrosis of obstructive nephropathy is most likely mediated by an increased level of Ang II in renal tissue.

Actins↗